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Clinical Reviews in Allergy & Immunology
Erschienen in: Clinical Reviews in Allergy & Immunology 1/2013

01.08.2013

Aspirin-Intolerant Asthma: A Comprehensive Review of Biomarkers and Pathophysiology

verfasst von: Juan R. Velazquez, Luis M. Teran

Erschienen in: Clinical Reviews in Allergy & Immunology | Ausgabe 1/2013

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Abstract

Aspirin-exacerbated respiratory disease is a tetrad of nasal polyps, chronic hypertrophic eosinophilic sinusitis, asthma, and sensitivity to aspirin. Unawareness of this clinical condition by patients and physicians may have grave consequences because of its association with near-fatal asthma. The pathogenesis of aspirin-intolerant asthma is not related with an immunoglobin E mechanism, but with an abnormal metabolism of the lipoxygenase (LO) and cyclooxygenase (COX) pathways. At present, a diagnosis of aspirin sensitivity can be established only by provocative aspirin challenge, which represents a health risk for the patient. This circumstance has encouraged the search for aspirin intolerance-specific biomarkers. Major attempts have focused on mediators related with inflammation and eicosanoid regulation. The use of modern laboratory techniques including high-throughput methods has facilitated the detection of dozens of biological metabolites associated with aspirin-intolerant asthma disease. Not surprisingly, the majority of these is implicated in the LO and COX pathways. However, substantial amounts of data reveal the participation of many genes deriving from different ontologies. Biomarkers may represent a powerful, noninvasive tool in the diagnosis of aspirin sensitivity; moreover, they could provide a new way to classify asthma phenotypes.
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Metadaten
Titel
Aspirin-Intolerant Asthma: A Comprehensive Review of Biomarkers and Pathophysiology
verfasst von
Juan R. Velazquez
Luis M. Teran
Publikationsdatum
01.08.2013
Verlag
Springer US
Erschienen in
Clinical Reviews in Allergy & Immunology / Ausgabe 1/2013
Print ISSN: 1080-0549
Elektronische ISSN: 1559-0267
DOI
https://doi.org/10.1007/s12016-012-8340-0

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